Department of Urology, Sapporo Medical University School of Medicine, Sapporo, Japan Department of Urology, Tohoku University Graduate School of Medicine, Sendai, Japan.
J Sex Med. 2011 Jul;8(7):1957-64. doi: 10.1111/j.1743-6109.2011.02283.x. Epub 2011 Apr 14.
The precise mechanisms underlying erectile dysfunction (ED) occurring after cavernous nerve (CN)-sparing surgery remain to be determined. Aim. To evaluate the expression of interleukin-6 (IL-6) and IL-6 receptor (IL-6R) after CN injury, and the effect of inhibiting IL-6 bioactivity on nerve injury-related ED.
Male Sprague-Dawley rats were divided into three groups: sham operation; bilateral CN dissection without crushing or cutting; and bilateral CN resection. In the interventional experiment, male rats underwent bilateral CN dissection, and anti-rat IL-6 antibody in phosphate-buffered saline (PBS) or vehicle alone was injected intraperitoneally immediately and 24 hours after CN dissection.
One, 3, 7, 28, and 56 days after surgery, the expression of IL-6 and IL-6R in the major pelvic ganglion (MPG) was examined by real-time polymerase chain reaction. In the interventional experiment, erectile function was assessed by determining intracavernous pressure divided by arterial pressure (ICP/AP) during electrical pelvic nerve stimulation at 4 weeks after surgery in the anti-IL-6-injected rats and PBS-injected rats. The degree of nerve injury was also evaluated by retrograde dye tracing with Fluorogold.
The expression levels of IL-6 and IL-6R were increased in the early period of CN injury, as compared with the sham group. IL-6 expression on day 1 was particularly enhanced. Four weeks after CN dissection, the anti-IL-6 group had greater ICP/AP and more FG-positive cells than the PBS group.
Expression levels of IL-6 in the MPG were increased in the acute phase following CN injury. Inhibition of IL-6 bioactivity attenuated ED following CN dissection. Thus, the suppression of excess inflammatory responses in the acute phase may lead to improvements in ED occurring after nerve-sparing radical prostatectomy.
阴茎勃起功能障碍（ED）发生的确切机制仍然需要确定。目的：评估海绵体神经（CN）保留手术后 IL-6 和 IL-6 受体（IL-6R）的表达，以及抑制 IL-6 生物活性对与神经损伤相关的 ED 的影响。
雄性 Sprague-Dawley 大鼠分为三组：假手术组；双侧 CN 解剖但不挤压或切割；双侧 CN 切除。在介入实验中，雄性大鼠接受双侧 CN 解剖，在 CN 解剖后立即和 24 小时，用磷酸盐缓冲液（PBS）中的抗大鼠 IL-6 抗体或单独的载体经腹腔内注射。
手术后 1、3、7、28 和 56 天，通过实时聚合酶链反应检测主要骨盆神经节（MPG）中 IL-6 和 IL-6R 的表达。在介入实验中，在手术后 4 周，用电刺激盆神经时，通过测量海绵体内压与动脉压的比值（ICP/AP）评估勃起功能，在抗 IL-6 注射大鼠和 PBS 注射大鼠中评估。用荧光金逆行标记法评估神经损伤程度。
与假手术组相比，CN 损伤早期 IL-6 和 IL-6R 的表达水平增加。CN 损伤后 1 天，IL-6 表达明显增强。CN 解剖后 4 周，抗 IL-6 组的 ICP/AP 高于 PBS 组，FG 阳性细胞较多。
MPG 中 IL-6 的表达水平在 CN 损伤后的急性期增加。抑制 IL-6 生物活性可减轻 CN 解剖后 ED。因此，在神经保留性根治性前列腺切除术后，抑制急性期过度炎症反应可能会改善 ED。
